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Patiromer for Patients With Heart Failure at Risk of Hyperkalemia: CARE-HK in HF Registry.

O. Cantu-Martinez,Stephen J Greene,13 Authors,Andrew J. Sauer

2026 · DOI: 10.1016/j.cardfail.2026.03.025
Journal of Cardiac Failure · 0 Citations

TLDR

In contemporary clinical practice, patiromer was associated with reducing sK+ but rates of RASi/mineralocorticoid receptor antagonist optimization remain low, and overcoming clinical inertia is required to optimize RASi/mineralocorticoid receptor antagonist therapy in patients with HF at high risk of HK.

Abstract

BACKGROUND

For patients with heart failure (HF), hyperkalemia (HK) may prevent optimal renin-angiotensin system inhibitor (RASi) use. Randomized trials show that patiromer, a contemporary potassium binder, reduces serum potassium (sK+) concentrations and HK, potentially enabling RASi optimization. We sought to assess the real-world effectiveness of patiromer in facilitating RASi optimization in HF patients at increased risk of HK.

METHODS AND RESULTS

The CARE-HK in HF (Cardiovascular and Renal Treatment in HF Patients with HK or at High Risk of HK) (NCT04864795) was a prospective registry of patients with chronic HF at increased risk of HK (prior or current HK or estimated glomerular filtration rate of <45 mL/min/1.73 m²). Patients treated with patiromer were propensity score matched with others not receiving potassium binders. HK episodes, sK+, and RASi optimization (≥50% target doses) were evaluated prospectively and retrospectively. Among 2558 patients, 234 (9.1%) received patiromer for a median of 12.0 months (interquartile range 6.0-19.4 months). Propensity matching yielded 211 patients treated with patiromer and 361 matched controls. The median patient age was 73 years (interquartile range 64-79 years); 79.4% were men, 50.2% had diabetes, and 44.9% had an estimated glomerular filtration rate of <45 mL/min/1.73 m². At patiromer initiation, the median sK+ was 5.5 mEq/L (interquartile range 5.4-5.7 mEq/L) and declined by 0.21 mEq/L (95% confidence interval 0.30-0.12 mEq/L) (P < .0001). However, RASi/mineralocorticoid receptor antagonist optimization within 2 years remained at ≤40% and did not increase with patiromer.

CONCLUSIONS

In contemporary clinical practice, patiromer was associated with reducing sK+ but rates of RASi/mineralocorticoid receptor antagonist optimization remain low. Overcoming clinical inertia, including the addition of patiromer when appropriate, is required to optimize RASi/mineralocorticoid receptor antagonist therapy in patients with HF at high risk of HK.